Pulmonary and Critical Care Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts 02115, USA.
Annu Rev Physiol. 2012;74:377-401. doi: 10.1146/annurev-physiol-020911-153348. Epub 2011 Oct 24.
(Macro)autophagy provides a membrane-dependent mechanism for the sequestration, transport, and lysosomal turnover of subcellular components, including proteins and organelles. In this capacity, autophagy maintains basal cellular homeostasis and healthy organelle populations such as mitochondria. During starvation, autophagy prolongs cell survival by recycling metabolic precursors from intracellular macromolecules. Furthermore, autophagy represents an inducible response to chemical and physical cellular stress. Increasing evidence suggests that autophagy, and its regulatory proteins, may critically influence vital cellular processes such as programmed cell death, cell proliferation, inflammation, and innate immune functions and thereby may play a critical role in the pathogenesis of human disease. The function of autophagy in disease pathogenesis remains unclear and may involve either impaired or accelerated autophagic activity or imbalances in the activation of autophagic proteins. This review examines the roles of autophagy in the pathogenesis of pulmonary diseases, with emphasis on pulmonary vascular disease and acute and chronic lung diseases.
（宏观）自噬提供了一种依赖于膜的机制，用于隔离、运输和溶酶体分解细胞内成分，包括蛋白质和细胞器。在这种能力下，自噬维持了基础细胞的内环境平衡和健康的细胞器群体，如线粒体。在饥饿时，自噬通过从细胞内大分子中回收代谢前体来延长细胞的存活时间。此外，自噬是对化学和物理细胞应激的诱导反应。越来越多的证据表明，自噬及其调节蛋白可能对程序性细胞死亡、细胞增殖、炎症和先天免疫功能等重要的细胞过程产生关键性影响，从而可能在人类疾病的发病机制中发挥关键作用。自噬在疾病发病机制中的作用尚不清楚，可能涉及自噬活性受损或加速，或自噬蛋白的激活失衡。这篇综述探讨了自噬在肺部疾病发病机制中的作用，重点关注肺血管疾病以及急性和慢性肺部疾病。
